Figure 2
Figure 2. CD48−/− HSCs show a defect in both short-term and long-term activity. (A) Donor chimerism in the peripheral blood measured with CD45.2 expression, from transplants of 100 000 donor WBM cells competed against 100 000 WT WBM cells. CD48−/− HSCs show a substantial transplantation defect (nonlinear regression analysis, P = .02061). (B) Lineage contribution of CD48−/− HSCs at 12 weeks. CD48−/− recipients show a slight but insignificant skewing toward the T-cell lineage at the cost of B cells. (C) Donor chimerism in the peripheral blood measured with CD45.2 expression, from competitive transplants of 300 000 WBM cells from either a CD48−/− mouse or WT mouse. CD48−/− HSCs still exhibit a substantial transplantation defect (nonlinear regression analysis, P < .01) at the higher BM dose. (D) Noncompetitive BM transplant with 300 000 CD48−/− or WT whole BM cells. Shown is the proportion of peripheral blood (CD45.1+) cells generated from the donor cells at the indicated time points (all error bars are SEM).

CD48−/− HSCs show a defect in both short-term and long-term activity. (A) Donor chimerism in the peripheral blood measured with CD45.2 expression, from transplants of 100 000 donor WBM cells competed against 100 000 WT WBM cells. CD48−/− HSCs show a substantial transplantation defect (nonlinear regression analysis, P = .02061). (B) Lineage contribution of CD48−/− HSCs at 12 weeks. CD48−/− recipients show a slight but insignificant skewing toward the T-cell lineage at the cost of B cells. (C) Donor chimerism in the peripheral blood measured with CD45.2 expression, from competitive transplants of 300 000 WBM cells from either a CD48−/− mouse or WT mouse. CD48−/− HSCs still exhibit a substantial transplantation defect (nonlinear regression analysis, P < .01) at the higher BM dose. (D) Noncompetitive BM transplant with 300 000 CD48−/− or WT whole BM cells. Shown is the proportion of peripheral blood (CD45.1+) cells generated from the donor cells at the indicated time points (all error bars are SEM).

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